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Carotid artery stenosis
Classification and external resources
ICD-10 I65.2
ICD-9 433.1
DiseasesDB 31178
MeSH D016893
The carotid artery is the large vertical artery in red. The blood supply to the carotid artery starts at the arch of the aorta (bottom). The carotid artery divides into the internal carotid artery and the external carotid artery. The internal carotid artery supplies the brain. Plaque often builds up at that division, and causes a narrowing (stenosis). Pieces of plaque can break off and block the small arteries above in the brain, which causes a stroke. Plaque can also build up at the origin of the carotid artery at the aorta.
Section of carotid artery with plaque. Blood flows from the common carotid artery (bottom), and divides into the internal carotid artery (left) and external carotid artery (right). The atherosclerotic plaque is the dark mass on the left.

Carotid stenosis is a narrowing or constriction of the inner surface (lumen) of the carotid artery, usually caused by atherosclerosis .

The carotid artery is the large artery whose pulse can be felt on both sides of the neck under the jaw. It starts from the aorta as the common carotid artery, and at the throat it forks into the internal carotid artery and the external carotid artery. The internal carotid artery supplies the brain, and the external carotid artery supplies the face. This fork is a common site for atherosclerosis, an inflammatory buildup of plaque that can narrow the common or internal artery.

The plaque can be stable and asymptomatic, or it can be a source of embolization. Emboli (solid pieces) break off from the plaque and travel through the circulation to blood vessels in the brain. As the vessel gets smaller, they can lodge in the vessel wall and restrict blood flow to parts of the brain that that vessel supplies. This ischemia can either be temporary giving a transient ischemic attack, or permanent resulting in a thromboembolic stroke.

Clinically, risk of stroke from carotid stenois is evaluated by the presence or absence of symptoms and the degree of stenosis on imaging.

Transient ischemic attacks (TIAs) are a warning sign, and are often followed by severe permanent strokes, particularly within the first two days. TIAs by definition last less than 24 hours (and usually last a few minutes), and usually take the form of a weakness or loss of sensation of a limb or the trunk on one side of the body, or loss of sight (amaurosis fugax) in one eye. Less common symptoms are artery sounds (bruits), or ringing in the ear (tinnitis).



Carotid stenosis is usually diagnosed by colour flow duplex ultrasound scan of the carotid arteries in the neck. This involves no radiation, no needles and no contrast agents that may cause allergic reactions. This test has moderate sensitivity and specificity, and yields many false-positive results.

Typically duplex ultrasound scan is the only investigation required for decision making (including proceeding to intervention) in carotid stenosis. Occasionally further imaging is required. One of several different imaging modalities, such as angiogram, computed tomography angiogram (CTA) or magnetic resonance imaging angiogram (MRA) may be useful. Each imaging modality has its advantages and disadvantages - the investigation chosen will depend on the clinical question and the imaging expertise, experience and equipment available.


The U.S. Preventive Services Task Force (USPSTF) recommends against screening for asymptomatic carotid artery stenosis in the general adult population.[1]


Options for treatment include:

The goal of treatment is to reduce the risk of stroke (cerebrovascular accident). Intervention (carotid endarterectomy or carotid stenting) can cause stroke, however where the risk of stroke from medical management alone is high, intervention may be beneficial. In selected, high-risk trial participants with asymptomatic severe carotid artery stenosis, carotid endarterectomy by selected surgeons reduces the 5-year absolute incidence of all strokes or perioperative death by approximately 5%. In excellent centers, carotid endarterectomy is associated with a 30-day stroke or mortality rate of about 3%; some areas have higher rates.[1]

Clinical guidelines (such as those of NICE)(NICE = (United Kingdom's) National Institute for Clinical Excellence) recommend that all patients with carotid stenosis be given medication, usually anti-hypertensive drugs, anti-clotting drugs, anti-platelet drugs (such as aspirin), and especially statins (which were originally prescribed for their cholesterol-lowering effects but were also found to reduce inflammation and stabilize plaque).

NICE and other guidelines also recommend that patients with symptomatic carotid stenosis be given carotid endarterectomy urgently, since the greatest risk of stroke is within days. Carotid endarterectomy reduces the risk of stroke or death from carotid emboli by about half.

For patients with stenosis but no symptoms, the surgical recommendations are less clear and controversial. Such patients have a historical risk of stroke of about 1-2% per year. Carotid endarerectomy has a surgical risk of stroke or death of about 2-4% in the best institutions. The Asymptomatic Carotid Surgery Trial (ASCT)(British Journal of Surgery, V.91,N.7,P.787-789, "The Asymptomatic Carotid Surgery Trial: bigger study, better evidence " Auth: Naylor AR), which started in 1993, reported in 2004 that carotid endarterectomy reduced major stroke and death by about half, even after surgical death and stroke was taken into account. However, the addition of statins to medical treatment has also lowered the stroke and death rate by so much that some surgeons believe that surgery no longer benefits patients. According to the Cochrane Collaboration ( ), the absolute benefit of surgery is small. (Cochrane Collaboration PDF - "Statins for acute ischemic stroke (Protocol)" by Squizzato A, Romualdi E, Dentali F, AgenoW )


  1. ^ a b Screening for Carotid Artery Stenosis. December 2007. U.S. Preventive Services Task Force. Agency for Healthcare Research and Quality, Rockville, MD.

See also



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